Expressional change of astrocytic Kir4.1 channel during epileptogenesis in audiogenic seizure-susceptible, Lgi1 mutant rats

Abstract

Background: Leucine-rich glioma-inactivated 1 (LGI1) was identified as a causative gene of autosomal dominant lateral temporal lobe epilepsy (ADLTE). We previously reported Lgi1 mutant rats, carrying a missense mutation (L385R), showed audiogenic seizure susceptibility. However, its mechanisms underlying seizure induction remain unknown. Astrocytes are recognized as an active partner of neurons in regulating neural activity. Specifically, dysfunction of astrocytic inwardly rectifying potassium (Kir) 4.1 channels mediating spatial potassium buffering is reported to be involved in the generation of generalized tonic-clonic seizures (GTCS).